X-ray Tomography Applied to Electrochemical Devices and Electrocatalysis.

X-ray computed tomography (CT) is a nondestructive three-dimensional (3D) imaging technique used for studying morphological properties of porous and nonporous materials. In the field of electrocatalysis, X-ray CT is mainly used to quantify the morphology of electrodes and extract information such as porosity, tortuosity, pore-size distribution, and other relevant properties. For electrochemical systems such as fuel cells, electrolyzers, and redox flow batteries, X-ray CT gives the ability to study evolution of critical features of interest in ex situ, in situ, and operando environments. These include catalyst degradation, interface evolution under real conditions, formation of new phases (water and oxygen), and dynamics of transport processes. These studies enable more efficient device and electrode designs that will ultimately contribute to widespread decarbonization efforts.

Insulin and IGF-1 receptors regulate complex I-dependent mitochondrial bioenergetics and supercomplexes via FoxOs in muscle.

Decreased skeletal muscle strength and mitochondrial dysfunction are characteristic of diabetes. The actions of insulin and IGF-1 through the insulin receptor (IR) and IGF-1 receptor (IGF1R) maintain muscle mass via suppression of forkhead box O (FoxO) transcription factors, but whether FoxO activation coordinates atrophy in concert with mitochondrial dysfunction is unknown. We show that mitochondrial respiration and complex I activity were decreased in streptozotocin (STZ) diabetic muscle, but these defects were reversed in muscle-specific FoxO1, -3, and -4 triple-KO (M-FoxO TKO) mice rendered diabetic with STZ. In the absence of systemic glucose or lipid abnormalities, muscle-specific IR KO (M-IR-/-) or combined IR/IGF1R KO (MIGIRKO) impaired mitochondrial respiration, decreased ATP production, and increased ROS. These mitochondrial abnormalities were not present in muscle-specific IR, IGF1R, and FoxO1, -3, and -4 quintuple-KO mice (M-QKO). Acute tamoxifen-inducible deletion of IR and IGF1R also decreased muscle pyruvate respiration, complex I activity, and supercomplex assembly. Although autophagy was increased when IR and IGF1R were deleted in muscle, mitophagy was not increased. Mechanistically, RNA-Seq revealed that complex I core subunits were decreased in STZ-diabetic and MIGIRKO muscle, and these changes were not present with FoxO KO in STZ-FoxO TKO and M-QKO mice. Thus, insulin-deficient diabetes or loss of insulin/IGF-1 action in muscle decreases complex I-driven mitochondrial respiration and supercomplex assembly in part by FoxO-mediated repression of complex I subunit expression.